Real-time 3-dimensional echocardiography provides new insight into mechanisms of tricuspid valve regurgitation in patients with hypoplastic left heart syndrome.

BACKGROUND: Tricuspid regurgitation in hypoplastic left heart syndrome has an impact on outcome, but its mechanisms remain unclear. METHODS AND RESULTS: Real-time 3-dimensional echocardiography was performed in 35 patients with hypoplastic left heart syndrome (age, 1 month to 10 years; 10 after first-stage Norwood, 12 after superior cavopulmonary shunt, 13 after Fontan). From the 3-dimensional data set, we marked the annulus in systole and diastole. At mid systole, we marked the location of the papillary muscle tip and point of chordal attachment to the leaflet. We traced the surfaces of the tricuspid valve leaflets and measured the volume of leaflet prolapse, tethering, annular and septal leaflet areas, and papillary muscle position. Seventeen patients had moderate tricuspid regurgitation (prolapse, 7; tethered leaflets, 7) and 18 mild (prolapse, 0; tethered leaflets, 7). Multiple linear regression analysis revealed that moderate tricuspid regurgitation is associated with leaflet tethering and prolapse; that in hypoplastic left heart syndrome with tethered leaflets, the papillary muscle is displaced laterally and the tricuspid annulus is more planar; and that enlargement of the annulus at mid systole, small septal leaflet area, and age affect the degree of prolapse. CONCLUSIONS: In hypoplastic left heart syndrome, moderate tricuspid regurgitation may be associated with increasing age, geometrical changes of the annulus, leaflet prolapse, lateral papillary muscle displacement, and subsequent leaflet tethering, as well as a smaller septal leaflet.

Short-term effect of monocuspid valves on pulmonary insufficiency and clinical outcome after surgical repair of tetralogy of Fallot.

In the surgical repair of tetralogy of Fallot, monocuspid valves are sometimes inserted within a transannular patch to prevent pulmonary insufficiency. To determine whether this monocuspid valve prevents short-term postoperative pulmonary insufficiency and improves clinical outcome, we reviewed clinical data and preoperative and postoperative echocardiographic variables from 61 patients who underwent one of three different procedures for repair of tetralogy of Fallot between August 1992 and March 1994. We compared features from 24 patients who had undergone transannular patch repair with a monocuspid valve (patch-valve) with those from 17 patients who had undergone patch repair without a monocuspid valve (patch) and 20 patients who had undergone repair without a transannular patch (no patch). We used the ratio of pulmonary valve insufficiency jet width to pulmonary artery diameter, as measured by color-flow Doppler flowmetry, as an index of severity of pulmonary insufficiency. Moderate to severe pulmonary insufficiency was arbitrarily defined as a ratio of at least 0.50. We found no significant differences in ratios among the patch-valve group (0.73 +/- 0.25, mean +/- standard deviation), the patch group (0.79 +/- 0.20), and the no patch group (0.59 +/- 0.23). The percentages of patients with moderate to severe pulmonary insufficiency did not differ among the three groups (patch-valve 80%, patch 90%, no patch 64%). Clinical data (including mortality, number of reoperations, intensive care unit and hospital lengths of stay, and postoperative hemodynamics) were similar in the three groups. We conclude that insertion of a monocuspid valve in repair of tetralogy of Fallot does not prevent short-term postoperative pulmonary insufficiency and does not improve immediate postoperative outcome for these patients.

Scimitar syndrome: twenty years' experience and results of repair.

BACKGROUND: Thirty-two patients with scimitar syndrome were seen in the period between 1975 and 1995. There were 11 male and 21 female patients. Median age at diagnosis was 7 months (mean 7.7 years, range 1 day to 70 years). Patients in whom the diagnosis was made during the first year of life (infantile group, n = 19) had more severe symptoms and had a higher incidence of heart failure (11/19 vs 0/13) and of pulmonary hypertension (11/19 vs 1/13) than did the patients in whom the diagnosis was made after age 1 year (adult group, n = 13). In 17 patients the anomalous pulmonary venous drainage was repaired by baffling the vein to the left atrium. The median age at this operation was 5.8 years (mean 14.8 years, range 6 months to 70 years). RESULTS: No deaths occurred in this surgical group during a mean follow-up period of 8.9 years (range 1.6 to 17 years). Eight patients (47%), however, had evidence of pulmonary venous stenosis after repair, and two required reoperation for pulmonary venous obstruction. All six children in the infantile group had postoperative pulmonary venous stenosis, compared with two of 11 older patients. Postoperative quantitative pulmonary perfusion scans performed in 15 patients demonstrated reduced flow to the right lung (24%, range 0% to 59%). CONCLUSION: We conclude that age at detection of scimitar syndrome is important in predicting outcome. Surgical repair seldom results in normal blood flow to the right lung but abolishes left-to-right shunt. Postoperative pulmonary venous obstruction is prevalent, especially in the infants.

The role of cardioplegic solution buffering in myocardial protection. A biochemical and histopathological assessment.

The advantages of buffering cardioplegic solutions to improve adenosine triphosphate preservation and postarrest hemodynamic function have been previously promoted. We evaluated the benefit of histidine buffering (195 mmol/L) in a low sodium (27 mEq/L) cardioplegic solution (Roe's) in a canine model of multidose cardioplegic arrest. Four solutions, two unbuffered (K+ = 10 mEq/L and K+ = 30 mEq/L) and two buffered (K+ = 10 mEq/L and K+ = 30 mEq/L), were tested in four groups of dogs for a 4 1/2 hour arrest period followed by 1 hour of reperfusion. Use of the unbuffered solution resulted in a drop in myocardial adenosine triphosphate from 29 +/- 1 mmol/kg (mean +/- standard error of the mean) (K+ = 30 mEq/L) and 28 +/- 2 mmol/kg (K+ = 10 mEq/L) to 8 +/- 2 mmol/kg and 7 +/- 2 mmol/kg, respectively, during the arrest period. In both buffered groups, adenosine triphosphate remained at preischemic levels during the entire arrest period. Myocardial glycogen followed the same pattern as adenosine triphosphate in the buffered groups. Lactate production was markedly elevated in all groups during ischemia. Postarrest hemodynamic function, as assessed by intraventricular isovolumic developed pressure measurements, was better (p less than 0.05) in the buffered low-potassium group than in the other three groups. The extent of myocardial necrosis, measured by triphenyl tetrazolium staining and confirmed by electron microscopy, was minimal (2% +/- 1% of biventricular mass) in the buffered low-potassium group, significantly greater (7% +/- 2% and 10% +/- 2%) in the unbuffered high-potassium and low-potassium groups, respectively, and highest (35% +/- 9%) in the buffered high-potassium group. These findings indicate that significant buffering capacity (similar to that of blood) in a crystalloid cardioplegic solution can be effective in preserving myocardial adenosine triphosphate stores, improving postarrest contractile function, and minimizing myocardial necrosis, provided the combination of high extracellular potassium and high pH levels is avoided.

Calcium paradox in an in vivo model of multidose cardioplegia and moderate hypothermia. Prevention with diltiazem or trace calcium levels.

The production and prevention of calcium paradox injury in myocardium was studied in a canine model of cardiopulmonary bypass with multidose, moderately hypothermic, crystalloid cardioplegic solution. During 4 1/2 hours of global ischemia, three groups of six dogs each received one of three histidine-buffered cardioplegic solutions (500 ml initially and 250 ml every 30 minutes) at 27 degrees C. Group 1 cardioplegic solution was calcium free, group 2 solution contained a trace amount of calcium chloride (70 mumols /L), and group 3 cardioplegic solution was calcium free but contained diltiazem (150 micrograms/kg body weight). Left ventricular function measured as percent control of developed pressure revealed significantly greater (p less than 0.05) recovery in groups 2 and 3. Triphenyltetrazolium chloride staining showed 35% +/- 9% (mean +/- standard error) of heart mass necrosis in group 1 versus 0% and 0.5% +/- 0.4% in groups 2 and 3, respectively (p less than 0.001). Electron microscopy revealed ultrastructural changes characteristic of calcium paradox injury in group 1 myocardium. Calcium paradox injury was produced in an in vivo model of global myocardial ischemia and multidose cardioplegia despite moderate hypothermia and non-coronary collateral flow. The addition of either trace levels of calcium or diltiazem to the cardioplegic solution was effective in preventing this injury.

Warm induction blood cardioplegia in the infant. A technique to avoid rapid cooling myocardial contracture.

The use of profound hypothermia and total circulatory arrest for repair of heart defects in neonates usually involves a period of systemic and myocardial bypass cooling. Rapid cooling of muscle (skeletal, smooth, and myocardial) can result in contracture through elevation of cytosolic calcium levels. The increased myocardial tone caused by cooling might render the heart more vulnerable to a subsequent period of cardioplegic ischemic arrest. Infants may be more susceptible to contracture because their small body mass allows more rapid myocardial temperature change when prearrest bypass cooling is used. The influence of avoiding rapid myocardial cooling before induced cardioplegic arrest was analyzed in a group of infants weighing less than 6 kg at the time of open cardiac operation. Myocardial ischemic arrest by warm (37 degrees C) induction blood cardioplegia was used in 57 infants and compared with results in 440 infants treated with standard blood cardioplegia. Multivariate logistic regression analysis revealed that patient diagnosis, weight, and age at operation were significant risk factors for operative mortality. The use of warm induction blood cardioplegia had a strongly positive independent effect on survival (p = 0.0003) for any patient weight, age, or diagnostic group. We recommend the avoidance of rapid myocardial cooling on bypass in all patients before induction of cardioplegic ischemic arrest.

Limiting edema in neonatal cardiopulmonary bypass with narrow-range molecular weight hydroxyethyl starch.

The marked edema observed in neonatal cardiopulmonary bypass is thought to result from pathologic increases in capillary permeability. Pentafraction is a subfraction of hydroxyethyl starch that is thought to be of appropriate size and shape to be retained by leaking capillaries and seal endothelial gaps in capillary basement membranes. To test the hypothesis that pentafraction would reduce edema in neonatal cardiopulmonary bypass, we established a model of edema formation in neonatal bypass in which neonatal piglets underwent 2 hours of normothermic cardiopulmonary bypass with crystalloid prime and no myocardial ischemia. Before initiation of bypass, experimental animals (n = 11) received intravenous pentafraction, 3 gm/kg. Control animals (n = 10) received an equivalent volume of saline. Hemodynamic parameters, animal weight, fluid redistribution, and percent tissue water of individual organs were assessed during and after bypass. Pentafraction treatment resulted in significant differences in (1) lowered percent body weight gain from baseline (11% versus 48%), (2) lowered volume requirement to maintain venous reservoir during cardiopulmonary bypass (148 ml/kg versus 581 ml/kg), (3) less fluid loss from the peritoneum (11 ml/kg versus 115 ml/kg), and (4) lowered percent tissue water of kidney, pancreas, stomach, jejunum, colon, and skeletal muscle (p less than 0.05 by unpaired t test). Pentafraction had no effect on hemodynamic parameters during bypass nor in percent tissue water of heart, lung, liver, spleen, skin, or brain. In summary, pentafraction lessened weight gain and fluid requirements during cardiopulmonary bypass, favorably influencing the percent tissue water of certain organs. If pentafraction functions as proposed, it may have wide applicability not only in cardiopulmonary bypass (or extracorporeal membrane oxygenation) but also in other clinical scenarios with altered capillary permeability.

Skeletal muscle extraaortic counterpulsation. A true arterial counterpulsation.

Reduction of left ventricular work load during systole, a critical component of arterial counterpulsation, has not previously been documented for skeletal muscle-powered extraaortic counterpulsation. To assess its capacity for afterload reduction, a skeletal muscle extraaortic counterpulsator was connected to the thoracic aorta and counterpulsated. Canine hearts (n = 7) were instrumented with left ventricular Millar catheters (Millar Instruments, Inc., Houston, Tex.) for pressure measurements and with piezoelectric ultrasonic crystals for measurement of the left ventricular minor axis dimension and wall thickness. During systole, skeletal muscle extraaortic counterpulsation resulted in a significant change in all three determinants of left ventricular circumferential wall stress compared with control conditions (no counterpulsation). Pressure decreased (peak systole, 100 +/- 5 versus 75 +/- 6 mm Hg; p less than 0.05 by paired t test), minor axis dimension decreased (end systole, 46.4 +/- 1.1 versus 45.8 +/- 1.1 mm; p less than 0.05 by paired t test), and wall thickness increased (end systole, 10.4 +/- 0.7 versus 10.6 +/- 0.7 mm; p less than 0.05 by paired t test). Left ventricular wall stress/dimension work loops showed a shift downward and to the left, a shift consistent with afterload reduction. The mean systolic left ventricular wall stress was significantly reduced, from 67.3 +/- 10.6 to 47.7 +/- 8.1 10(3) dyne/cm2 (p less than 0.05 by paired t test). Skeletal muscle extraaortic counterpulsation increased the diastolic aortic pressure from 72 +/- 6 to 105 +/- 8 mm Hg (p less than 0.05 by paired t test). Our data, which documented the counterpulsator's direct effects on left ventricular functional mechanics, showed that skeletal muscle extraaortic counterpulsation is capable of both diastolic augmentation of arterial pressure and systolic unloading of the left ventricle. Skeletal muscle extraaortic counterpulsation has potential application for ventricular unloading in the treatment of chronic end-stage heart failure.

The recognition, identification of morphologic substrate, and treatment of subaortic stenosis after a Fontan operation. An analysis of twelve patients.

Twelve children were identified with subaortic stenosis after Fontan's operation. All had absent resting and isoproterenol-provoked pressure gradient before the Fontan procedure. Six had a univentricular heart of left ventricular morphology, three had a single ventricle of right ventricular morphology, one had tricuspid atresia with transposition of the great arteries, one had pulmonary atresia, intact ventricular septum, and hypoplastic right ventricle, and one had corrected transposition with hypoplastic systemic ventricle. The median interval between the Fontan operation and the recognition of subaortic stenosis was 2.5 years. Ten patients underwent surgical treatment after a prior Fontan operation: Five had myectomy and enlargement of ventricular septal defect with two operative deaths; two had placement of a valved conduit from the ventricular apex to the descending aorta, and both died postoperatively; two with single ventricle had subaortic myectomy, and one had enlargement of ventricular septal defect and pulmonary aortic connection. Complete heart block developed in only one patient. Postoperative testing with Doppler echocardiography with color flow imaging demonstrated good relief of subaortic stenosis. All six children who survived the operation are well 4 months to 4 years later. Subaortic stenosis is a progressive lesion that may develop after a Fontan operation. Its surgical treatment continues to carry a significant mortality. Myectomy and enlargement of ventricular septal defect achieve direct relief of the obstruction with minimal risk of heart block.

Subaortic stenosis in the spectrum of atrioventricular septal defects. Solutions may be complex and palliative.

UNLABELLED: From July 1982 through September 1994, 19 children had operative treatment of subaortic stenosis associated with an atrioventricular septal defect. Specific diagnosis were septum primum defects in 7, Rastelli type A defects in 6, transitional defects in 4, inlet ventricular septal defect with malattached chordae in 1, and tetralogy of Fallot with Rastelli type C defect in 1. Twenty-seven operations for subaortic stenosis were performed. Surgical treatment of the outlet lesion was performed at initial atrioventricular septal defect repair in 3 children and in the remaining 16 from 1.2 to 13.1 years (mean 4.9 years, median 3.9 years) after repair. Eighteen of the 19 children had fibrous resection and myectomy for relief of obstruction. Seven children had an associated left atrioventricular valve procedure. One child received an apicoaortic conduit. Seven children (36.8%) required 8 reoperations for previously treated subaortic stenosis. Time to the second procedure was 2.8 to 7.4 years (mean 4.9 years). Follow-up is 0.4 to 14.0 years (median 5.6 years). Six-year actuarial freedom from reoperation is 66% +/- 15%. The angle between the plane of the outlet septum and the plane of the septal crest was measured in 10 normal hearts (86.4 +/- 13.7) and 10 hearts with atrioventricular septal defects (22.2 +/- 26.0; p < 0.01). The outflow tract can be effectively shortened, widened, and the angle increased toward normal by augmenting the left side of the superior bridging leaflet and performing a fibromyectomy. CONCLUSION: Standard fibromyectomy for subaortic stenosis in children with atrioventricular septal defects leads to a high rate of reoperation. Leaflet augmentation and fibromyectomy may decrease the likelihood of reoperation.

Superior vena cava to pulmonary artery anastomosis: an adjunct to biventricular repair.

From May 1981 to September 1995, 38 patients received a superior vena cava-pulmonary artery anastomosis in association with biventricular repair. Patients were divided into four groups on the basis of indication for operation. Group A (19 patients) had a small physiologic right ventricle defined by tricuspid anulus z values or predicted right ventricular volume. Group B (11 patients) had a functionally compromised right ventricle. Group C (four patients) consisted of those receiving a superior vena cava-pulmonary artery anastomosis as a facilitation to biventricular repair. Group D (four patients) was defined by acute postoperative right ventricular dysfunction. Age ranged from 5 months to 51 years (median 3.5 years). There were 14 different underlying primary diagnoses in this cohort and multiple associated anomalies. Operative mortality was as follows: group A, two of 19 (10.5%); group B, two of 11 (18%); group C, none of four (0%); and group D, three of four (75%). Follow-up is complete in 37 of 38 patients (97%), ranging from 1 to 174 months (mean 46.3 +/- 36.9). Twenty-two patients are in New York Heart Association functional class I and eight patients are in class II. No clinical evidence of cyanosis or protein-losing enteropathy has been detected. With the use of this adjunctive approach, acceptable intermediate-term outcomes were obtained in patients having an anatomically or functionally compromised pulmonary ventricle. The anastomosis safely facilitates repair in a subset of patients. Results for this procedure when used as a salvage operation for right ventricular dysfunction have not been satisfactory.

Rapid cooling contracture of the myocardium. The adverse effect of prearrest cardiac hypothermia.

Hypothermic total circulatory arrest for repair of congenital heart lesions in neonates requires a period of rapid core cooling on cardiopulmonary bypass during which the myocardium is also exposed to hypothermic perfusion. Myocardial hypothermia in the nonarrested state results in an increase in contractility due to elevation of intracellular calcium levels. This study was designed to test the hypothesis that rapid myocardial cooling before cardioplegic ischemic arrest results in damage, with impaired recovery during reperfusion. Two groups of 10 rabbit hearts were perfused on an isolated Langendorff apparatus. Group N (normothermia) was perfused at 37 degrees C before 2 hours of cardioplegic ischemic arrest at 10 degrees C. Group C (cooling) was perfused at 15 degrees C in the unarrested state for 20 minutes before the same cardioplegic arrest conditions as group N. Left ventricular isovolumic pressure measurements, biochemical measurements from right ventricular biopsy specimens, and ventricular necrosis as defined by tetrazolium staining were used to compare the groups at 30 and 60 minutes of normothermic reperfusion. Developed pressure at a constant volume was preserved in group N at 90.7 +/- 4.5 mm Hg versus 76.9 +/- 6.3 in group C after reperfusion (p less than 0.05). Diastolic compliance showed significant deterioration in group C, with marked elevation of diastolic pressure during reperfusion (group N = 6.8 +/- 2.5 mm Hg versus group C = 38.9 +/- 6.1 after reperfusion; p less than 0.001). Adenosine triphosphate levels were significantly higher in group N both at end-ischemia and after reperfusion versus group C (group N = 17.0 +/- 1.1 nmol/mg protein versus group C = 7.7 +/- 1.0 after reperfusion; p less than 0.001). Group N had 0.4% +/- 0.4% necrosis of ventricular mass versus 19.3% +/- 2.2% with prearrest cooling in group C (p less than 0.0001). These results indicate that, when combined with cardioplegic ischemic arrest, rapid myocardial cooling in the unarrested state results in significant damage. The mechanism may be related to the cytosolic calcium loading effect of hypothermia that is not relieved during the subsequent period of cardioplegic arrest. Although hypothermia is an essential component to ischemic preservation, rapid cooling contracture can adversely influence cardioplegic myocardial protection.

Experience with repair of congenital heart defects using adjunctive endovascular devices.

The use of endovascular devices as an adjunct to repair of congenital heart anomalies represents a novel but unproven therapeutic approach. Intraoperative implantation of pulmonary arterial stents (5 to 15 mm diameter) was done in 11 patients with pulmonary atresia with ventricular septal defect (n = 4), classic tetralogy of Fallot (n = 2), truncus arteriosus (n = 1), hypoplastic left heart syndrome (stage II [n = 1] and stage III [n = 1] Norwood procedure), and miscellaneous pulmonary arterial stenoses (n = 3), as well as in patients with congenital (n = 1) and postoperative (n = 3) pulmonary venous obstruction and in 1 patient with combined pulmonary arterial and venous obstruction. The stents were effective at achieving immediate patency in all patients. There were two early deaths, one related to acute thrombosis of a small-diameter left pulmonary artery stent. Reintervention because of stent-related pulmonary arterial stenosis was frequently necessary. In five of seven patients who survived more than 1 month after implantation of stent size 8 mm or smaller severe stent-related pulmonary arterial obstruction developed. In four of the five patients with pulmonary vein stent implantation intractable obstruction developed, resulting in death in all three patients who had bilateral pulmonary vein stent implantation. Intraoperative occlusion of apical muscular ventricular septal defect with use of a clamshell device inserted from the right atrial approach was accomplished in four patients. One patient who underwent associated aortic arch reconstruction died as a result of left ventricular hypoplasia. The results in the remaining three patients were favorable on the basis of absence of significant late residual intraventricular shunting, left ventricular dysfunction, or arrhythmia. We conclude that recurrent intraluminal obstruction as a result of neointimal hyperplasia appears to be an eventual certainty in currently designed small-diameter endovascular stents. For this reason, we would recommend standard surgical techniques for repair of obstructive lesions of the pulmonary arterial confluence to maximize growth potential. Device occlusion of muscular ventricular septal defects is feasible but probably only indicated for complex cases of ventricular septal deficiency that otherwise necessitate a left ventriculotomy.

Effects of hyperkalemia on neonatal endothelium and smooth muscle.

BACKGROUND: Contradictory results have been reported regarding the effect of hyperkalemic cardioplegic or organ preservation solutions on endothelial and smooth muscle cells. The present study was designed to determine the effects of potassium concentrations and exposure times to hyperkalemia on endothelium-derived relaxing factor (nitric oxide) biosynthesis and release, and smooth muscle function in neonatal vessels. METHODS: Aortic rings taken from neonatal rabbits were studied in organ baths at physiologic pressure. The effect of Krebs' solution containing 5, 25, 50, or 100 mmol/L potassium incubated for 45 minutes (group 1), St. Thomas' Hospital cardioplegic solution containing 16, 25, 50, or 100 mmol/L potassium for 45 minutes (group 2), and Krebs' solution containing 5 and 50 mmol/L potassium or St. Thomas' Hospital cardioplegic solution containing 16 and 50 mmol/L potassium for 135 minutes (group 3) or 270 minutes (groups 4 and 5) was examined. The rings were then washed and contracted with U46619 (30 nmol/L). The ability to release endothelium-derived relaxing factor (nitric oxide) in response to acetylcholine was tested. RESULTS: The maximal relaxation induced by acetylcholine did not decrease in any group. Evidence of slight alteration of smooth muscle contraction was seen only in the rings incubated in Krebs' solution with 50 mmol/L potassium for 270 minutes (group 4) with unchanged maximal contraction and sensitivity to potassium (group 5). CONCLUSIONS: We conclude that after exposure for a limited time (4 1/2 hours), hyperkalemia per se does not significantly alter the function of endothelium to release endothelium-derived relaxing factor (nitric oxide) in response to acetylcholine and only slightly alters the contraction speed of smooth muscle in the neonatal rabbit aorta.

Hemodynamic alteration by fetal surgery accelerates myocyte proliferation in fetal guinea pig hearts.

BACKGROUND: Fetal heart development occurs by hyperplasia as myocytes lose the capacity to proliferate at birth. This potential for cell division may have application in altering fetal growth patterns in congenital cardiac malformations, but it is not known whether the proliferative activity can be modified by intrauterine surgical manipulation. The purpose of this study was to determine whether hemodynamic alteration by fetal surgery influences myocyte proliferation and myocardial development. METHODS: Six pregnant guinea pigs of 50 to 52 days of gestation (term, 65 days) underwent hysterotomy, and the fetal ascending aorta was banded and narrowed by 50% (AoB). Cesarean section was performed near term, and the heart was assessed for myocyte proliferative activity (Ki-67 monoclonal antibody), apoptosis, and morphologic features. RESULTS: The heart to body weight ratio (1.02% +/- 0.12% versus 0.42% +/- 0.02%, p < 0.01) and left ventricular posterior wall thickness (1.89 +/- 0.25 mm versus 1.31 +/- 0.19 mm, p < 0.01) were significantly higher in the AoB group. The percentage of Ki-67 positive cells was increased in AoB group (29.5% +/- 4.4% versus 15.3% +/- 1.3% in right ventricle, 35.8% +/- 5.1% versus 13.1% +/- 1.7% in interventricular septum, and 39.8% +/- 3.2% versus 12.0% +/- 2.0% in left ventricle (p < 0.01). The apoptotic cell to myocyte ratio was less than 1/1000 in both groups. CONCLUSIONS: Fetal hemodynamic alteration by aortic banding accelerates myocardial cellular proliferation without affecting apoptosis, suggesting that in utero cardiac interventions have a greater influence on myocardial development compared with postnatal intervention.

Asanguineous reperfusion in a canine model of cardiopulmonary bypass and controlled postischemic work.

This study was designed to test the hypothesis that asanguineous reperfusion with a standard crystalloid cardioplegic solution results in improved myocardial salvage after a period of global ischemia. Four groups of 6 dogs each were placed on cardiopulmonary bypass. Control group A (work only) performed two hours of controlled work by contracting against a saline-filled left intraventricular balloon. Control group B (ischemia only) underwent 45 minutes of global normothermic ischemia before simple blood reperfusion while supported on bypass. Groups C and D were subjected to ischemia and reperfusion as in group B, followed by controlled work stress as in group A. Group D, however, received 500 mL of St. Thomas' Hospital solution immediately before blood reperfusion. Morphological analysis showed no significant injury in groups A and B, whereas group C had 11.4% +/- 2.4% necrosis of heart mass versus 2.5% +/- 1.1% in group D (p less than 0.001). Biochemical data from left ventricular biopsies showed no significant differences between groups B, C, and D. Functional analyses showed deterioration of diastolic compliance in group C (p less than 0.05), although a significant difference in systolic functional indexes could not be detected. Myocardial protection and salvage was improved by initial reperfusion with an asanguineous cardioplegic solution versus reperfusion with blood alone.

Pulmonary atresia with intact ventricular septum: results of the Fontan procedure.

BACKGROUND: Children with pulmonary atresia and an intact ventricular septum show a heterogeneous spectrum of cardiac anomalies. A biventricular repair is attainable in some; a Fontan procedure or a one-and-a-half ventricle is the only possible repair for others. Children with right ventricle-to-coronary artery connections, with or without right ventricle-dependent coronary artery blood flow, are a high-risk group. METHODS: Between May 1980 and December 1994, 22 children underwent a Fontan operation for the treatment of pulmonary atresia with an intact ventricular septum at The Hospital for Sick Children, Toronto. The mean age was 5.8 years (median, 4.9 years). All children had had at least one pre-Fontan palliative procedure; 19 had two, and 7 of these had three or more. Right ventricle-to-coronary artery connections were present in 15 children, including 5 with right ventricle-dependent coronary artery blood flow. Thromboexclusion of the right ventricle was done in 10 children, with 7 undergoing it before and 3 at the time of the Fontan procedure. RESULTS: There were three early deaths (13.6%) and one late death. The actuarial survival at 10 years after the Fontan operation was 80%. Early postoperative complications occurred in 4 children. Follow-up was completed in all children at a mean of 4 years (range, 1 to 12.5 years) after the Fontan operation. Atrial arrhythmia occurred in 3 children, and permanent pacemakers were required in 4. CONCLUSIONS: Results of the Fontan operation for the treatment of pulmonary atresia with an intact ventricular septum are satisfactory. Thromboexclusion of the right ventricle is indicated in the presence of right ventricle-to-coronary artery connections without right ventricle-dependent coronary artery blood flow. The right ventricle should not be decompressed or thromboexcluded in children with right ventricle-dependent coronary artery blood flow, and at the Fontan operation, saturated blood must enter the right ventricle.

Tolerance of epicardial coronary endothelium and smooth muscle to hyperkalemia.

Results of previous studies have suggested that high K+ concentrations in cardioplegic solutions may be detrimental to coronary endothelium in perfused hearts, as determined from changes in the coronary flow rate, but the direct functional changes in endothelium secondary to hyperkalemia have not been fully studied. To determine the effect of the K+ concentration in a physiologic solution (Krebs') and in St. Thomas' cardioplegic solution, and the effect of exposure time on endothelium and smooth muscle, porcine coronary artery rings were set up in organ baths under a physiologic pressure. The effect of exposure to Krebs' solution containing 5.9 or 50 mmol/L K+ or to St. Thomas' solution containing 16 or 50 mmol/L K+, for either 2 hours (group I) or 4 hours (group II), was examined. The solutions were continuously aerated with 95% oxygen and 5% carbon dioxide to exclude the effects of ischemia and hypoxia. The rings were then washed and contracted with K+ (25 mmol/L). The ability to release endothelium-derived relaxing factor (EDRF) in response to an EDRF stimulus (substance P) was used as an index of endothelial function. Smooth muscle function was evaluated in terms of the K(+)-induced contraction force and the relaxation induced with glyceryl trinitrate, in addition to the maximal substance P-induced relaxation. The maximal relaxation induced by substance P did not decrease by incubation with 50 mmol/L K+ in any group (p > 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Survival analysis of infants under age 18 months presenting with tetralogy of Fallot.

The trend to perform early primary repair of tetralogy of Fallot prompted us to review our experience in the current era with the traditional protocol consisting of palliation during infancy, if required, and repair after infancy. During a 10-year period, 270 infants with tetralogy of Fallot presented aged less than 18 months. Thirteen infants (4.8%) had major noncardiac lesions that precluded definitive care for their congenital heart disease. Twenty infants (7.4%) had major associated cardiac lesions (atrioventricular septal defect or absent pulmonary valve syndrome, or both). Survival in this group was poor, with only 58% +/- 12% reaching the age of 10 years. Four of the seven deaths occurred before intracardiac repair was performed. The remaining 237 infants presented with isolated tetralogy of Fallot. Eight-nine percent +/- 2.3% survived to age 10 years. Sixty percent of these infants required palliation, and survival in these infants did not differ from that in those who never required palliation. However, 19 infants (8%) required palliation in the first month of life. In these children, survival to age 10 years was significantly lower (77%), secondary palliation was frequently required (n = 11), and a transannular patch or conduit at the time of repair (10 of 14 patients) was more likely needed than it was in children who had not undergone a palliative procedure during the neonatal period. The survival in infants with tetralogy of Fallot is unlikely to be different, regardless of whether primary repair or a staged repair is carried out. The quality of survival, including the exercise capability and absence of arrhythmias, must be assessed to determine which protocol is superior.

Superior myocardial preservation with modified UW solution after prolonged ischemia in the rat heart.

Cardiac transplantation remains constrained by poor graft tolerance of prolonged cold ischemia. University of Wisconsin solution has remarkably extended ischemic preservation in pancreas, kidney, and liver transplantation. To assess its efficacy in cardiac preservation, modified University of Wisconsin solution flush and storage were tested against St. Thomas' cardioplegia flush and normal saline solution storage after six hours of ischemia at 0 degrees C in 46 isolated rat hearts. After ischemia, groups were compared before and after reperfusion. After ischemia but before reperfusion, University of Wisconsin solution hearts had significantly less tissue water (3.8%), superior tissue sodium, potassium, calcium, and magnesium profiles, and elevated adenosine and inosine levels, and tended toward better histological preservation. After reperfusion, University of Wisconsin solution more effectively preserved left ventricular compliance (75% versus 35% of baseline), developed pressure (71% versus 45% of baseline), histological integrity, and tissue potassium and calcium profiles than St. Thomas' solution. The University of Wisconsin solution provided superior preservation of systolic and diastolic ventricular function, tissue histology, tissue water, and tissue electrolytes than did St. Thomas' cardioplegia and normal saline solution storage in this experimental model, and might result in improved graft tolerance of ischemia in clinical cardiac transplantation.